Patients with intestinal diseases leading to steatorrhea have hyperabsorption of dietary oxalate and hyperoxaluria. Malabsorption syndromes have intraluminal and mucosal defects leading to enhanced absorption of oxalate. The intraluminal defects result from sequestration of calcium by malabsorbed fatty acids leading to formation of soluble exalate salts within the lumen of the bowel which are absorbed by passive diffusion. Investigations suggest that the colon is the primary site of hyperabsorption of oxalate. We have demonstrated that addition of calcium to the diet can suppress oxalate absorption by favoring formation of calcium oxalate within the lumen of the bowel. Additional investigations are planned to evaluate the effect of other binding agents such as magnesium in preventing absorption by alteration of intraluminal solubility of oxalate. It has recently been shown that malabsorption syndromes also lead to altered colonic permeability as a result of exposure of the colonic mucosa to malabsorbed free fatty acids and bile salts. Thus, in a setting of low intraluminal calcium ion concentrations not only is there formation of soluble oxalate salts, but the colonic mucosa is more permeable to oxalate after nonspecific changes in its permeability characteristics as a result of exposure to bile salts and fatty acids. Investigations are planned to determine whether the permeability defect is the result of intracellular or intercellular changes. On the basis of clinical investigations, management of patients with intestinal disease who have calcium oxalate nephrolithiasis can be summarized as follows: 1) a low oxalate diet, 2) a low fat diet, 3) modest calcium intake (750 mg/day), 4) Cholestyramine, and 5) medium chain triglycerides. BIBLIOGRAPHIC REFERENCE: Stauffer, J.Q.: Hyperoxaluria and Calcium Oxalate Nephrolithiasis after Jejunoileal Bypass. Am. J. Clinic. Nutrition, 1976 (In press).